Electrical stimulation of Nucleus Ambiguus (NA) and of Lateral Hypothalamus (LH) produces a sympathetic response that partly inhibits insulin secretion in anesthetized rats in vivo. This inhibitory component is accompanied by a stimulatory one that can, in both cases, be revealed by the infusion of an alpha-blocker to the rats. The analogy between the stimulatory effect on insulin secretion due to NA or LH electrical stimulation is only partial. Indeed the NA-induced insulin secretion is abolished by vagotomy, while that induced by LH stimulation appears to be mediated by possible release of humoral factor(s). Acute bilateral lesions of the ventromedial hypothalamus (VMH) in anesthetized rats produce, within minutes, an hyperinsulinemia that is abolished by superimposed vagotomy. Semi-chronic (7 d.) lesions of the VMH in rats result in changes in the activity of their subsequently isolated perfused pancreases. Indeed, and compared to controls, pancreases from VMH-lesioned rats oversecrete insulin and glucagon while undersecreting somatostatin. Such alterations due to lesions of the VMH appear to be the result of increased vagal activity and (possibly via a trophic effect of the nerve) of increased cholinergic (muscarinic) receptors. CNS organisation of genetically obese (ob/ob) mice is abnormal when compared to controls. Abnormalities are mainly a relative increase of the size of neurons of the LH and the dorsomotor nucleus of the vagus (DMX), compared to that of other CNS neurons. These abnormalities could conceivably play a role in the genesis of hyperinsulinemia of these animals.

Animals↗

PubMedDate not supplied

Defective diet-induced but normal cold-induced brown adipose tissue adaptation in hypothalamic obesity in rats.

our weeks after bilateral ventromedial hypothalamic (VMH) lesions in the female rat reared at 23 degrees C, the weight of the interscapular brown adipose tissue (IBAT) was doubled as compared to appropriate controls. Tested in vitro, the tissue of the lesioned animals showed, per unit weight, a basal and a noradrenaline--or octanoate--stimulated heat output about half of that of the tissue from the controls. However, basal and stimulated heat outputs as well as beta-oxidative capacity of IBAT from lesioned animals and their appropriate controls were the same when calculated per whole fat pad. The lesioned animals were hyperphagic, with a gross energy intake 70% larger than that of the controls. Cold acclimation at 5 degrees C for 3 weeks was found to restore the basal and stimulated heat outputs per unit weight of IBAT of the lesioned animals to the level of that of their cold acclimated controls. The weight of the tissue did not change significantly in lesioned animals upon cold exposure whereas controls exhibited the expected hypertrophy. Calculated per whole fat pad, the stimulated heat output became 33% larger in lesioned animals than in appropriate controls. The total beta-oxidative capacity increased by 3 fold in controls and 4.8 fold in lesioned animals. Cold exposure was followed by a mean increase of gross energy intake of 43% in the controls and 31% in the lesioned animals as compared to their gross energy intake at 23 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗